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Hypertonic saline resuscitation decreases central NO inhibitory tone and improves the AVP response to hemorrhagic shock in alcohol intoxicated rodents
Author(s) -
Sulzer Jesse Kyle,
Whitaker Annie M,
Molina Patricia E
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.849.4
Acute alcohol intoxication (AAI) impairs the hemodynamic response to hemorrhagic shock (HS) and fluid resuscitation (FR) with lactated Ringer's (LR) and attenuates the HS‐induced rise in plasma arginine vasopressin (AVP). Studies suggest that AAI enhances nitric oxide (NO) inhibitory tone in the paraventricular nucleus (PVN) contributing to a blunted AVP response to HS. In contrast, AAI does not impair the AVP response to hypertonic saline (HTS), which we predict is due to suppressed PVN NO levels in AAI non‐HS animals. Thus, we hypothesized that FR with HTS would decrease NO in the PVN and enhance AVP release leading to improved blood pressure (MABP) recovery in AAI‐HS. Male Sprague Dawley rats received a 15h alcohol infusion (2.5g/kg + .3g/kg/h) or isovolumic dextrose (DEX) followed by HS (40mmHg × 60 min) and FR with HTS (7.5%; 4ml/kg) or LR (2.4x blood volume removed). HTS decreased NO in the PVN and enhanced (~66%) circulating AVP vs LR in AAI‐ and DEX‐HS 2h post‐FR. HTS improved initial MABP recovery vs LR in AAI (109 vs 80 mmHg) and DEX (114 vs 83 mmHg). Peripheral V 1a antagonism prior to FR prevented the pressor effect of HTS, while only delaying MABP recovery in LR‐treated animals. These results suggest that resuscitation with HTS in AAI+HS removes central inhibition of NO restoring circulating AVP and that the pressor effect of HTS is dependent on stimulation of AVP release. DOD‐PR‐054196, NIAAA‐7577, NIAAA‐19587.